Branching morphogenesis is a key process utilized by many organs during embryonic development, but its mechanisms are not clearly understood. The developing submandibular salivary gland provides an excellent model system for clarifying the mechanisms comprising this phenomenon. Here we describe a recently developed set of approaches currently being used to identify and characterize molecules necessary for branching morphogenesis. The combination of laser microdissection with T7-SAGE is reviewed as a method for gene discovery of candidate molecules that may be essential for early organ morphogenesis. We describe a current approach that promises to improve our understanding of the early morphological changes that occur during branching morphogenesis. This knowledge should facilitate development of future tissue engineering techniques and approaches to regenerating branching organs.

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Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein (MAP) kinase kinase kinase that activates the JNK and p38 MAP kinase cascades. ASK1 has a broad range of biological activities including cell differentiation and stress-induced apoptosis. Recently, we have shown that endogenous ASK1 constitutively forms a high molecular mass complex, which we designate “ASK1 signalosome”. Here we introduce this novel signaling complex as a key regulator of cell fate in response to oxidative stress.

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Nuclear factor-κB (NF-κB) is one of the most important transcription factors for survival, activation, and proliferation of immune cells. Main pathway of NF-κB for T cell activation is known to be NF-κB1/RelA classical pathway. Meanwhile, the role of NF-κB2/RelB non-classical pathway is still unclear. A number of reports as to knockout mice for NF-κB subunits can lead to understand in vivo functions of NF-κB. Moreover, some autoimmune models have been described in knockout and mutant mice of NF-κB genes and NF-κB-associated genes. Thus, NF-κB might be one of potent factors for pathogenesis of autoimmune diseases. This article reviews each function of NF-κB subunits as to immune system, mainly T cell activation based on our recent study and previous published studies.

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Head formation requires the simultaneous inhibition of multiple caudalizing signals during early vertebrate embryogenesis. Elucidation of molecular mechanisms that establish the anterior-posterior axis of body patterning as well as the nervous system is a major topic in development. Recently, we have identified a novel antagonist against Wnt and FGF signaling for head formation, Shisa, which functions cell-autonomously in the endoplasmic reticulum (ER). Shisa suppresses the processes of protein maturation and cellular transportation of Wnt and FGF receptors in ER, thereby inhibiting both signaling pathways. Thus, the study of Shisa provide new molecular concepts for signaling regulation in which cells control the establishment of particular signaling components in ER.

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Long-term bone marrow (BM) repopulating (LTR)-hematopoietic stem cells (HSCs) exist frequently in BM trabecular bone surfaces, and it was clarified that osteoblasts (OBs) are critical for sustaining HSCs. The interaction of HSCs with their particular microenvironments, known as stem cell niches, is critical for maintaining their stem cell properties, including self-renewal capacity and the ability to differentiate into single or multiple lineages. In the niche, the fates of HSCs are regulated by the signaling molecules, extracellular matrix, and cell adhesion molecules produced by osteoblasts. Interaction of HSCs with their stem cell niches is critical for cell cycle regulation of HSCs. Especially, the quiescence of the cell cycle is thought to be an indispensable property for the maintenance of HSCs. We demonstrate that HSCs expressing the receptor tyrosine kinase Tie2 are quiescent and anti-apoptotic, transplantable and comprise a side-population (SP) of HSCs, which contact closely with angiopoietin-1 (Ang-1), a ligand for Tie2, expressing osteoblasts in the BM niche. The interaction of Tie2 and Ang-1 regulates the functional criteria of HSCs in the BM niche, including quiescence, anti-apoptosis and cell adhesion.

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The present report focuses on a review of A) the parasympathetic vasodilator fibers in the orofacial skin, B) the central mechanism by which trigeminal stimulation elicits parasympathetic reflex vasodilatation, and C) the presence of parasympathetic vasodilator fibers in the jaw muscles. A) The parasympathetic neurons, particularly those running as efferents in the glossopharyngeal nerve, were involved in vasodilatation elicited by stimulation of the infra-orbital nerve and the maxillary buccal gingiva. Furthermore, the vasodilator response was not affected by lesion of the pterygopalatine ganglion, suggesting that reflex vasodilatation is mediated via the otic ganglion but not via the pterygopalatine ganglion. B) The trigeminal spinal nucleus is an important bulbar relay for lingual nerve-evoked parasympathetic reflex vasodilatation in the lower lip. C) There are parasympathetic cholinergic and non-cholinergic vasodilator fibers originating from cell bodies in the otic ganglion in the rat masseter muscle, and that these fibers are reflexly activated by trigeminal afferent nerve stimulation. The physiological function of the parasympathetic vasodilator fibers in the orofacial area is unknown. However, it has recently been suggested that the trigeminal system may participate in autonomic and behavioral functions such as feeding and drinking. The present review adds a new facet to the evidence that there is a close link between parasympathetic vasodilator fibers and the trigeminal system in the facial area.

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Numerous investigations based on observations of the enamel structures have reported that ameloblast movement develops the arrangement of enamel prisms leading to the formation of the Hunter-Schreger bands. Cytological and immunocytological examinations of ameloblasts were also shown ameloblast motility is involved in producing the Hunter-Schreger bands and prism arrangement. However, these conclusions were based on only the enamel structures or the location of ameloblasts. In the present study, we observed direct evidence that ameloblast groups consisted of a variety of arrangements of ameloblasts, which were concerned with the zones corresponding to the Hunter-Schreger bands in the same section of Indian elephant molar tooth germ.
Initially there were cell masses that appeared in the dental papilla under the undifferentiated inner enamel epithelium. In the next developmental stage , these clusters disappeared and were replaced by groups of inner enamel epithelial cells concerned with the stratum intermedium and the stellate reticulum, and finally extending to the outer enamel epithelial cells groups. These groups correspond to the various zones of the Hunter-Schreger bands.
These results provide the initial signs that “ameloblast grouping and dancing” arises in the dental papilla and that the motility is produced by a harmonious and combined movement of the whole enamel organ, moving the enamel structures.

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Histological and histometric evaluations were done to investigate the effects of streptozotocin-induced diabetes on peri-implant tissue after osseointegration in the rat maxilla. Titanium screw implants were immediately inserted into the sockets after extraction of left upper first molars of 4-week-old male Wistar rats. Rats were divided into three groups. Rats in groupI and groupII were sacrificed at 4 and 8 weeks after implantation, respectively, and rats in group DM, in which streptozotocin was injected intraperitoneally at 4 weeks after implantation, were sacrificed at 8 weeks after implantation. Histological and histometric evaluations were carried out for decalcified specimens with EDTA and undecalcified ground specimens. Newly formed bone contacted the implant surface directly in the three groups. No significant difference in the bone-implant contact rate was found among the three groups. However, moderate inflammatory cell invasion and dilatation of capillaries were observed in the proper lamina around the implants. The bone height was significantly less in the DM group than in groupI, while significance was not found between group DM and groupII. These results suggested that hyperglycemia for 4 weeks after osseointegration affected the marginal bone level, whereas it did not influence the bone-implant contact rate.

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The purpose of this study was to investigate the effect of the duration of hyperglycemia on the osseointegration and bone formation around titanium implants. Rats were divided in to three groups, the short-term-hyperglycemia group (group S), the long-term-hyperglycemia group (group L), and the control group. In groups S and L, hyperglycemia was induced with streptozotocin 2 and 6 weeks before implantation, respectively. Rats received titanium implants in their femora, and were sacrificed 1, 2, 4, and 8 weeks after implantation. In the control group, the newly formed bone that directly contacted the implant surface increased with time. In groups S and L, fibrous connective tissue was observed on some parts of the implants. There were significant differences in bone-implant contact among the three groups at 4 weeks after implantation. Newly formed bone including the bone fragments scattered by surgery was remodeled, becoming thinner with time in the control group, whereas it remained immature, away from the implant in groups S and L. Although there were significant differences in the number of TRAP-positive cells between the control group and the hyperglycemia groups, there was no significant difference between groups S and L. It is suggested that the duration of hyperglycemia affected osseointegration around titanium implants.

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